Dilated cardiomyopathy is characterized by an enlarged and poorly contracting left ventricle. The main causes include inflammatory, toxic, metabolic, inherited, idiopathic and miscellaneous factors. On evaluation, patients typically present with decreased cardiac output, tachycardia and signs of congestion. Tests include echocardiogram, which shows increased left ventricular size and reduced ejection fraction, and ECG, which may show conduction delays. Treatment focuses on managing symptoms with diuretics and blocking neurohormonal activation to prevent worsening, while devices like ICDs are used in eligible patients.
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Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
Cardiomyopathy (KAR-de-o-mi-OP-ah-thee) refers to diseases of the heart muscle. These diseases have many causes, signs and symptoms, and treatments.
In cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid. In rare cases, the muscle tissue in the heart is replaced with scar tissue.
As cardiomyopathy worsens, the heart becomes weaker. It's less able to pump blood through the body and maintain a normal electrical rhythm. This can lead toheart failure or irregular heartbeats called arrhythmias (ah-RITH-me-ahs). In turn, heart failure can cause fluid to build up in the lungs, ankles, feet, legs, or abdomen.
The weakening of the heart also can cause other complications, such as heart valve problems.
OverviewThe main types of cardiomyopathy are:
Dilated cardiomyopathy
Hypertrophic (hi-per-TROF-ik) cardiomyopathy
Restrictive cardiomyopathy
Arrhythmogenic (ah-rith-mo-JEN-ik) right ventricular dysplasia
(dis-PLA-ze-ah)
Other types of cardiomyopathy sometimes are referred to as "unclassified cardiomyopathy."
Cardiomyopathy can be acquired or inherited. "Acquired" means you aren't born with the disease, but you develop it due to another disease, condition, or factor. "Inherited" means your parents passed the gene for the disease on to you. Many times, the cause of cardiomyopathy isn't known.
Cardiomyopathy can affect people of all ages. However, people in certain age groups are more likely to have certain types of cardiomyopathy. This article focuses on cardiomyopathy in adults.
OutlookSome people who have cardiomyopathy have no signs or symptoms and need no treatment. For other people, the disease develops quickly, symptoms are severe, and serious complications occur.
Treatments for cardiomyopathy include lifestyle changes, medicines, surgery, implanted devices to correct arrhythmias, and a nonsurgical procedure. These treatments can control symptoms, reduce complications, and stop the disease from getting worse.
National Heart Lung and Blood Institute
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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2. Definition
Cardiomyopathies are defined as
"a heterogeneous group of diseases of the
myocardium associated with mechanical
and/or electrical dysfunction that usually (but
not invariably) exhibit inappropriate ventricular
hypertrophy or dilatation and are due to a
variety of causes that frequently are genetic."
4. Dilated Cardiomyopathy
•An enlarged left ventricle with decreased systolic function
as measured by left ventricular ejection fraction
characterizes dilated cardiomyopathy .
• Systolic failure is more marked
• Diastolic dysfunction, in the setting of marked volume
overload
6. Pathophysiology
Brief primary injury such as infection or toxin exposure.
Some myocytes may die during the initial injury, while
others survive only to have later programmed cell death,
(apoptosis).
As the surviving myocytes hypertrophy to accommodate
the increased burden of wall stress,
Local and circulating factors stimulate deleterious
responses that contribute to progression of disease,
even in the absence of further primary injury,Dynamic
remodeling and the amount of ventricular dilation.
Mitral regurgitation commonly develops as the valvular
apparatus is distorted by ventricular dilation
7.
8. DCM: Inflammatory
Infective
Reported with almost all types of infectious agents
Viral- Co xsackie , adenovirus, HIV, hepatitis C
Parasitic - T. cruzi— Chag as' dise ase , toxoplasmosis
Bacterial- diphtheria, Spirochetal ,Bo re llia
Rickettsial-Q fever
Fungal -with systemic infection
10. DCM: Inflammatory
Mechanism
Direct tissue injury resulting from viral infection
Immune mediated injury
Viral infection in susceptible hosts may be a
proximate cause of cardiomyopathy
11. DCM: Peripartum
Diagnostic Criteria
1 mo pre, 6 mos post
Echo: LV dysfunction
LVEF < 45%
LVEDD > 2.7 cm/m2
Epidemiology/Etiology
1:4000 women
Riskfactors - increased maternal age, increased
parity, twin pregnancy, malnutrition, use of
tocolytic therapy for premature labor, and
preeclampsia or toxemia of pregnancyJAMA
12. DCM: Peripartum
Proposed mechanisms:
Inflammation - reflect increased susceptibility
to viral myocarditis or
Autoimmune -myocarditis due to cross-
reactivity of anti-uterine antibodies against
cardiac muscle.
prolactin cleavage fragment, salt ingestion
Women with full recovery are more likely to
tolerate a subsequent pregnancy than are
14. DCM: Toxic
Alcoholic cardiomyopathy
Toxicity is attributed both to alcohol and acetaldehyde.
Superimposed vitamin deficiencies and toxic a additives
are rarely implicated.
6 drinks daily for 5–10 years, but frequent binge
drinking may also be sufficient.
Reversible with abstinence
Mechanism?:
Myocyte cell death and fibrosis
Directly inhibits: mitochondrial oxidative
phosphorylation Fatty acid oxidation
15. DCM: Toxic
Anthracyclines
Cause vacuolar degeneration and myofibrillar loss.
Generation of reactive oxygen species involving heme
compounds is currently the favored explanation for myocyte
injury and fibrosis.
Disruption of the large titin protein may contribute to loss of
sarcomere organization.
Three different presentations
Acute heart failure/ Early onset /The chronic presentation -
Leads to a relatively nondilated ventricle, perhaps due to
fibrosis.
Thus, the stroke volume may be severely reduced with an
ejection fraction of 30–40%,
Therapy is suppression of "inappropriate" sinus tachycardia,
and attention to postural hypotension .
21. DCM: Idiopathic
Is a diagnosis of exclusion,
when all other known factors have been
excluded.
two-thirds of dcm are still labeled as
idiopathic;
may reflect unrecognized genetic disease.
Continued reconsideration of etiology often
reveals later
22. Miscellaneous
Arrhythmogenic RV Dysplasia
Desmosomal complex disrupt myocyte junctions
and adhesions,
Myocardium of RV free wall replaced:
Fibrofatty tissue
Regional wall motion/function is reduced
Ventricular arrhythmias
SCD in young
"woolly hair," and thickened palms and soles.
24. Miscellaneous
LV Noncompaction
Diagnostic Criteria
Prominent trabeculations, deep recesses in LV apex
Thin compact epicardium, thickened endocardium
associated with multiple genetic variants in the sarcomeric
and other proteins such as tafazzin
Prognosis and Treatment
Increased risk of CHF, VT/SCD, thrombosis
Hereditary risk
Screening of offspring
26. Miscellaneous
Tako-Tsubo Cardiomyopathy
The apical ballooning syndrome, or stress-induced
cardiomyopathy, occurs typically
In older women after sudden intense emotional or
physical stress
Presentations include pulmonary edema, hypotension,
and chest pain with ECG changes mimicking an acute
infarction.
May result from intense sympathetic activation with
heterogeneity of myocardial autonomic innervation,
diffuse microvascular spasm, and/or direct
catecholamine toxicity.
28. Evaluation of the DCM
HISTORY
Detailed family history
History of alcohol, illicit drugs, chemotherapy or radiation
therapy
A past or associated history of rheumatologic, endocrine, or
infectious diseases
Assessment of ability to perform routine and desired
activities
Assessment of volume status, orthostatic blood pressure,
body mass index
32. X-RAY CHEST
Cardiomegaly
Pulmonary vascular
congestion
Kerley B lines
Prominent
vasculature of the
upper lung fields.
Pleural effusion
usually on the right
side, but it can be
bilateral
33. Electrocardiogram
No specific electrocardiographic findings
Sinus tachycardia is often present
poor R wave progression, intraventricular conduction
delays, and LBBB.
A wide QRS complex portends a worse prognosis
left ventricular fibrosis may exhibit anterior Q waves
nonspecific ST-segment and T wave abnormalities as
well as P wave alterations
Persistent supraventricular or ventricular
tachyarrhythmias represent an important etiologic factor
for ventricular dysfunction
34. ECHOCARDIOGRAPHY.
Cornerstone in the evaluation and
management
LVEDD are usually greater than 60 mm
Global hypokinesia
Decreased EF and FS
Associated ds
36. CARDIAC MRI AND MULTIDETECTOR CT
RADIONUCLIDE IMAGING
INVASIVE EVALUATION INCLUDING
ENDOMYOCARDIAL BIOPSY.
37. Management
PHARMACOLOGIC ANDDEVICE THERAPY
Neurohormonal antagonists to prevent
disease progression
Diuretics to maintain the volume balance are
the therapeutic cornerstone
Prophylactic implantable cardiac defibrillators
and biventricular pacemakers is indicated in
appropriate patients
39. SURGERY.
Patients with structural heart ds conditions
corrected
Left ventricular assist devices- provide
aggressive mechanical support to patients
with advanced decompensated heart failure
EMERGING SPECIFIC THERAPIES
infections and immunomodulatory agents
Stem cells for cardiac regeneration and gene
40. Presentation with Symptomatic Cardiomyopathy
Dilated Restrictive Hypertrophic
Ejection fraction
(normal 55%)
Usually <30% 25-50% >60%
LVDD (nor<55 mm) 60 mm >60 mm (may be
decreased)
Often decreased
Left ventricular wall
thickness
Decreased Normal or increased Markedly increased
Atrial size Increased Increased; may be
massive
Increased; related to
abnormal
Valvular
regurgitation
Related to annular
dilation; mitral earlier,
during
decompensation;
tricuspid late stages
Related to endocardial
involvement; frequent
mitral and tricuspid
regurgitation, rarely
severe
Related to valve-
septum interaction;
mitral regurgitation
Common first
symptoms
Exertional intolerance Exertional intolerance,
fluid retention early
Exertional intolerance;
may have chest pain
The threshold of left ventricular enlargement and dysfunction necessary to diagnose peripartum cardiomyopathy has not been precisely defined. The following definition, based upon a 1992 NHLBI workshop definition for idiopathic dilated cardiomyopathy, has been proposed [34,35]:
Left ventricular ejection fraction (LVEF) less than 45 percent AND/OR M-mode fractional shortening less than 30 percent PLUS Left ventricular end-diastolic dimension greater than 2.7 cm/m2